The metabolism of ethanol is directly related to oxidative stress, and its ingestion leads to the formation of reactive oxygen species (ROS) such as hydroxyl radicals, superoxide and hydrogen peroxide. Vitamin E has been widely used as an antioxidant; when administered in large doses it is deposited in the liver and then excreted in the bile, urine and feces. The objective of the present study was to evaluate the rate of excretion of fecal vitamin E in relation to its concentrations in serum and liver, and its role as a protective antioxidant against DNA damage induced by acute ethanol consumption. Wistar rats were divided into four groups receiving food and water ad libitum for 4 days plus the following treatments: Control (CG, n = 10 ) no treatment; Ethanol (ET, n = 10 ), receiving an acute ethanol dose intraperitoneally in the amount of 5 g/kg; vitamin E (VE, n = 10) receiving a high oral dose of vitamin E within the first three days in the amount of 100 tocopherol mg/kg body weight; ethanol plus vitamin E (VE + ET, n = 10 ) receiving both the ethanol and vitamin E doses. Higher concentrations of vitamin E were observed in the blood and liver of the animals in the groups that received vitamin E supplementation, independent of the presence or absence of ethanol. Concomitantly, these groups were also those with the highest concentration of the vitamin in the stool. The rate of DNA damage was higher in the groups that received ethanol with or without supplemental vitamin E. However, the rate of damage was lower in the group that received vitamin E supplementation than in the group that did not. The present results show that vitamin E has a protective effect against DNA damage induced by ethanol by reducing the extent of DNA damage.